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Advances in Osteogenesis

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 8770

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Dr. Andrea Del Fattore

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Bone Physiopathology Research Unit, Genetics and Rare Diseases Research Division, Bambino Gesù Children’s Hospital, IRCCS, 00165 Rome, Italy
Interests: bone; osteoblast; osteoclast; bone formation; bone erosion; bone disease
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Dear Colleagues,

Alterations in bone formation activity leads to the onset of several bone diseases characterized by increased or reduced bone mass; the consequence of the unbalanced bone formation can be, in some cases, lethal.

Understanding the molecular and cellular mechanisms controlling the osteogenesis process is important to dissect the pathways involved in bone formation and to identify new therapeutic approaches for rare bone diseases. Moreover, osteogenesis is essential for the mechanisms of bone healing or fracture healing; thus, in this field, the bone scientific community aims to use 3D bioprinting technology for the reconstruction of bone segments, printing bone surfaces and cells including mesenchymal stem cells and osteoblasts.

The aim of this Special Issue is to collect reports regarding the characterization of new mechanisms and pathways involved in bone formation that could be important for the identification of new therapeutic approaches for patients with altered bone mass or with fractures. Original research, reviews, opinion papers, or short communications are welcome.

Dr. Andrea Del Fattore
Guest Editor

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Keywords

osteogenesis
osteoblast
bone formation
disease
bone

Published Papers (7 papers)

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Research

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16 pages, 2955 KiB

Open AccessArticle

Selenium Lessens Osteoarthritis by Protecting Articular Chondrocytes from Oxidative Damage through Nrf2 and NF-κB Pathways

by Hsiao-Ling Cheng, Chia-Chi Yen, Li-Wen Huang, Yu-Chen Hu, Tzu-Ching Huang, Bau-Shan Hsieh and Kee-Lung Chang

Int. J. Mol. Sci. 2024, 25(5), 2511; https://doi.org/10.3390/ijms25052511 - 21 Feb 2024

Viewed by 739

Abstract

Osteoarthritis (OA) causes joint pain and disability due to the abnormal production of inflammatory cytokines and reactive oxygen species (ROS) in chondrocytes, leading to cell death and cartilage matrix destruction. Selenium (Se) intake can protect cells against oxidative damage. It is still unknown whether Se supplementation is beneficial for OA. This study investigated the effects of Se on sodium iodoacetate (MIA)-imitated OA progress in human chondrocyte cell line (SW1353 cells) and rats. The results showed that 0.3 μM of Se treatment could protect SW1353 cells from MIA-induced damage by the Nrf2 pathway by promoting the gene expression of glutathione-synthesis-related enzymes such as the glutamate–cysteine ligase catalytic subunit, the glutamate–cysteine ligase modifier subunit, and glutathione synthetase. In addition, glutathione, superoxide dismutase, glutathione peroxidase, and glutathione reductase expressions are also elevated to eliminate excessive ROS production. Moreover, Se could downregulate NF-κB, leading to a decrease in cytokines, matrix proteases, and glycosaminoglycans. In the rats, MIA-induced cartilage loss was lessened after 2 weeks of Se supplementation by oral gavage; meanwhile, glutathione synthesis was increased, and the expressions of pro-inflammatory cytokines were decreased. These results suggest that Se intake is beneficial for OA due to its effects of decreasing cartilage loss by enhancing antioxidant capacity and reducing inflammation. Full article

(This article belongs to the Special Issue Advances in Osteogenesis)

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16 pages, 5236 KiB

Open AccessArticle

Surface Modification of Polylactic Acid Bioscaffold Fabricated via 3D Printing for Craniofacial Bone Tissue Engineering

by Yao-Chang Liu, Guan-Jie Lo, Victor Bong-Hang Shyu, Chia-Hsuan Tsai, Chih-Hao Chen and Chien-Tzung Chen

Int. J. Mol. Sci. 2023, 24(24), 17410; https://doi.org/10.3390/ijms242417410 - 12 Dec 2023

Viewed by 891

Abstract

Bone tissue engineering is a promising solution for advanced bone defect reconstruction after severe trauma. In bone tissue engineering, scaffolds in three-dimensional (3D) structures are crucial components for cell growth, migration, and infiltration. The three-dimensional printing technique is well suited to manufacturing scaffolds since it can fabricate scaffolds with highly complex designs under good internal structural control. In the current study, the 3D printing technique was utilized to produce polylactic acid (PLA) scaffolds. BMSCs were seeded onto selected scaffolds, either hydrogel-mixed or not, and cultivated in vitro to investigate the osteogenic potential in each group. After osteogenic incubation in vitro, BMSC-seeded scaffolds were implanted onto rat cranium defects, and bone regeneration was observed after 12 weeks. Our results demonstrated that BMSCs were able to seed onto 3D-printed PLA scaffolds under high-resolution observation. Real-time PCR analysis showed their osteogenic ability, which could be further improved after BMSCs were mixed with hydrogel. The in vivo study showed significantly increased bone regeneration when rats’ cranium defects were implanted with a hydrogel-mixed BMSC-seeded scaffold compared to the control and those without cell or hydrogel groups. This study showed that 3D-printed PLA scaffolds are a feasible option for BMSC cultivation and osteogenic differentiation. After mixing with hydrogel, BMSC-seeded 3D-printed scaffolds can facilitate bone regeneration. Full article

(This article belongs to the Special Issue Advances in Osteogenesis)

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12 pages, 3702 KiB

Open AccessArticle

Col1A-2 Mutation in Osteogenesis Imperfecta Mice Contributes to Long Bone Fragility by Modifying Cell-Matrix Organization

by Grégoire André, Antoine Chretien, Antoine Demoulin, Mélanie Beersaerts, Pierre-Louis Docquier and Catherine Behets

Int. J. Mol. Sci. 2023, 24(23), 17010; https://doi.org/10.3390/ijms242317010 - 30 Nov 2023

Cited by 1 | Viewed by 724

Abstract

Osteogenesis imperfecta (OI) is a rare congenital bone dysplasia generally caused by a mutation of one of the type I collagen genes and characterized by low bone mass, numerous fractures, and bone deformities. The collagen organization and osteocyte lacuna arrangement were investigated in the long bones of 17-week-old wildtype (WT, n = 17) and osteogenesis imperfecta mice (OIM, n = 16) that is a validated model of severe human OI in order to assess their possible role in bone fragility. Fractures were counted after in vivo scanning at weeks 5, 11, and 17. Humerus, femur, and tibia diaphyses from both groups were analyzed ex vivo with pQCT, polarized and ordinary light histology, and Nano-CT. The fractures observed in the OIM were more numerous in the humerus and femur than in the tibia, whereas the quantitative bone parameters were altered in different ways among these bones. Collagen fiber organization appeared disrupted, with a lower birefringence in OIM than WT bones, whereas the osteocyte lacunae were more numerous, more spherical, and not aligned in a lamellar pattern. These modifications, which are typical of immature and less mechanically competent bone, attest to the reciprocal alteration of collagen matrix and osteocyte lacuna organization in the OIM, thereby contributing to bone fragility. Full article

(This article belongs to the Special Issue Advances in Osteogenesis)

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12 pages, 3363 KiB

Open AccessArticle

Deubiquitinase USP17 Regulates Osteoblast Differentiation by Increasing Osterix Protein Stability

by Myeong Ji Kim, Meiyu Piao, Yuankuan Li, Sung Ho Lee and Kwang Youl Lee

Int. J. Mol. Sci. 2023, 24(20), 15257; https://doi.org/10.3390/ijms242015257 - 17 Oct 2023

Cited by 1 | Viewed by 833

Abstract

Deubiquitinases (DUBs) are essential for bone remodeling by regulating the differentiation of osteoblast and osteoclast. USP17 encodes for a deubiquitinating enzyme, specifically known as ubiquitin-specific protease 17, which plays a critical role in regulating protein stability and cellular signaling pathways. However, the role of USP17 during osteoblast differentiation has not been elusive. In this study, we initially investigated whether USP17 could regulate the differentiation of osteoblasts. Moreover, USP17 overexpression experiments were conducted to assess the impact on osteoblast differentiation induced by bone morphogenetic protein 4 (BMP4). The positive effect was confirmed through alkaline phosphatase (ALP) expression and activity studies since ALP is a representative marker of osteoblast differentiation. To confirm this effect, Usp17 knockdown was performed, and its impact on BMP4-induced osteoblast differentiation was examined. As expected, knockdown of Usp17 led to the suppression of both ALP expression and activity. Mechanistically, it was observed that USP17 interacted with Osterix (Osx), which is a key transcription factor involved in osteoblast differentiation. Furthermore, overexpression of USP17 led to an increase in Osx protein levels. Thus, to investigate whether this effect was due to the intrinsic function of USP17 in deubiquitination, protein stabilization experiments and ubiquitination analysis were conducted. An increase in Osx protein levels was attributed to an enhancement in protein stabilization via USP17-mediated deubiquitination. In conclusion, USP17 participates in the deubiquitination of Osx, contributing to its protein stabilization, and ultimately promoting the differentiation of osteoblasts. Full article

(This article belongs to the Special Issue Advances in Osteogenesis)

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12 pages, 3137 KiB

Open AccessArticle

BMP-9 Improves the Osteogenic Differentiation Ability over BMP-2 through p53 Signaling In Vitro in Human Periosteum-Derived Cells

by Jin-Ho Park, Eun-Byeol Koh, Young-Jin Seo, Hye-Seong Oh and June-Ho Byun

Int. J. Mol. Sci. 2023, 24(20), 15252; https://doi.org/10.3390/ijms242015252 - 17 Oct 2023

Cited by 3 | Viewed by 1017

Abstract

Bone morphogenetic proteins (BMPs) have tremendous therapeutic potential regarding the treatment of bone and musculoskeletal disorders due to their osteo-inductive ability. More than twenty BMPs have been identified in the human body with various functions, such as embryonic development, skeleton genesis, hematopoiesis, and neurogenesis. BMPs can induce the differentiation of MSCs into the osteoblast lineage and promote the proliferation of osteoblasts and chondrocytes. BMP signaling is also involved in tissue remodeling and regeneration processes to maintain homeostasis in adults. In particular, growth factors, such as BMP-2 and BMP-7, have already been approved and are being used as treatments, but it is unclear as to whether they are the most potent BMPs that induce bone formation. According to recent studies, BMP-9 is known to be the most potent inducer of the osteogenic differentiation of mesenchymal stem cells, both in vitro and in vivo. However, its exact role in the skeletal system is still unclear. In addition, research results suggest that the molecular mechanism of BMP-9-mediated bone formation is also different from the previously known BMP family, suggesting that research on signaling pathways related to BMP-9-mediated bone formation is actively being conducted. In this study, we performed a phosphorylation array to investigate the signaling mechanism of BMP-9 compared with BMP-2, another influential bone-forming growth factor, and we compared the downstream signaling system. We present a mechanism for the signal transduction of BMP-9, focusing on the previously known pathway and the p53 factor, which is relatively upregulated compared with BMP-2. Full article

(This article belongs to the Special Issue Advances in Osteogenesis)

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Review

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12 pages, 721 KiB

Open AccessReview

Effect of Hyperprolactinemia on Bone Metabolism: Focusing on Osteopenia/Osteoporosis

by Soo Jin Yun, Hyunji Sang, So Young Park and Sang Ouk Chin

Int. J. Mol. Sci. 2024, 25(3), 1474; https://doi.org/10.3390/ijms25031474 - 25 Jan 2024

Viewed by 1274

Abstract

Prolactin is a hormone secreted from lactotroph cells in the anterior pituitary gland to induce lactation after birth. Hyperprolactinemia unrelated to lactation is a common cause of amenorrhea in women of a childbearing age, and a consequent decrease in the gonadotropin-releasing hormone (GnRH) by a high prolactin level can result in decreased bone mineral density. Osteoporosis is a common skeletal disorder characterized by decreased bone mineral density (BMD) and quality, which results in decreased bone strength. In patients with hyperprolactinemia, changes in BMD can be induced indirectly by the inhibition of the GnRH–gonadal axis due to increased prolactin levels or by the direct action of prolactin on osteoblasts and, possibly, osteoclast cells. This review highlights the recent work on bone remodeling and discusses our knowledge of how prolactin modulates these interactions, with a brief literature review on the relationship between prolactin and bone metabolism and suggestions for new possibilities. Full article

(This article belongs to the Special Issue Advances in Osteogenesis)

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22 pages, 1796 KiB

Open AccessReview

Molecular and Cellular Mechanisms of Osteoporosis

by Ivan V. Zhivodernikov, Tatiana V. Kirichenko, Yuliya V. Markina, Anton Y. Postnov and Alexander M. Markin

Int. J. Mol. Sci. 2023, 24(21), 15772; https://doi.org/10.3390/ijms242115772 - 30 Oct 2023

Cited by 5 | Viewed by 2566

Abstract

Osteoporosis is a widespread systemic disease characterized by a decrease in bone mass and an imbalance of the microarchitecture of bone tissue. Experimental and clinical studies devoted to investigating the main pathogenetic mechanisms of osteoporosis revealed the important role of estrogen deficiency, inflammation, oxidative stress, cellular senescence, and epigenetic factors in the development of bone resorption due to osteoclastogenesis, and decreased mineralization of bone tissue and bone formation due to reduced function of osteoblasts caused by apoptosis and age-depended differentiation of osteoblast precursors into adipocytes. The current review was conducted to describe the basic mechanisms of the development of osteoporosis at molecular and cellular levels and to elucidate the most promising therapeutic strategies of pathogenetic therapy of osteoporosis based on articles cited in PubMed up to September 2023. Full article

(This article belongs to the Special Issue Advances in Osteogenesis)

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